Acid Transport

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Olivier Bonny - One of the best experts on this subject based on the ideXlab platform.

Giovanni E. Mann - One of the best experts on this subject based on the ideXlab platform.

  • Amino Acid Transport by small intestinal, hepatic, and pancreatic epithelia
    Gastroenterology, 1995
    Co-Authors: Mark E. Mailliard, Bruce R. Stevens, Giovanni E. Mann
    Abstract:

    M'ovement of nutrients (amino Acids and sugars) into ~and out of cells is predominantly mediated by plasma membrane-bound activities that represent the function of discrete Transport proteins. Amino Acid Transporters are by convention referred to as Transport systems. Figure 1 shows the known mammalian amino Acid Transport systems in the small intestine, liver, and pancreas. Amino Acid Transport systems are understood primarily in terms of their functional activity with a striking void of knowledge regarding protein structure and composition. Because identification of the complimentary DNAs (cDNAs) or proteins responsible for the activity of most of the individual amino Acid Transport systems is lacking, some caution is necessary when assigning each system its own status as an integral membrane protein. In this review of amino Acid Transport, the authors will assume that confirmation of the protein structure of the Transport systems awaits only their molecular characterization, which is an area of much recent progress. This review will report on the Transport systems for L--amino Acids present in the plasma membrane of epithelial cells of the small intestine, liver, and pancreas. To present a comprehensive overview that includes recent investigation, each of the individual sections of the review will highlight somewhat different but complimentary aspects of the understanding of amino Acid Transport. The reader is referred to other recent excellent reviews on the subject) -6

  • Significance of γ-glutamyltranspeptidase in exocrine pancreatic amino Acid Transport
    Biochimica et biophysica acta, 1991
    Co-Authors: Juan Sastre, J.h. Sweiry, K. Doolabh, Jose Viña, Giovanni E. Mann
    Abstract:

    The exocrine pancreas is rich in gamma-glutamyltranspeptidase (GGT, EC 2.3.2.2) and exhibits high rates of amino Acid Transport and protein synthesis. The role of the gamma-glutamyl cycle in mediating neutral amino Acid Transport in the isolated perfused rat pancreas was investigated using acivicin, an inhibitor of GGT, and a rapid dual isotope dilution technique. When treatment in vivo with acivicin (50 mg/kg) was followed 1 h later by continuous perfusion of the isolated pancreas with 10-mu-M acivicin, GGT levels decreased from 53 +/- 3 IU/g to 4.9 +/- 1.5 IU/g. This marked inhibition of GGT activity was not associated with decreased uptake for either L-alanine or L-glutamine, suggesting that the gamma-glutamyl cycle plays a negligible role in amino Acid Transport across the basolateral membrane of the pancreatic epithelium.

Aurélie Edwards - One of the best experts on this subject based on the ideXlab platform.

H C Blair - One of the best experts on this subject based on the ideXlab platform.

  • Tyrosine kinase inhibitor effects on avian osteoclastic Acid Transport
    The American Journal of Clinical Nutrition, 1998
    Co-Authors: J P Williams, S E Jordan, S Barnes, H C Blair
    Abstract:

    We found that tyrosine kinase pp60 c-scr coisolates with Acid-Transporting osteoclast membranes and hypothesized that this kinase regulates hydrochloric Acid Transport. We assayed the membrane Acid Transport and bone degradation effects of tyrosine kinase inhibitors in avian osteoclasts. Isoflavone, tyrphostin, and benzoquinonoid inhibitors were compared with inactive analogues to determine nonspecific effects. Acid-secreting membranes, isolated by nitrogen cavitation, were assayed as reconstituted vesicles by using acridine orange to indicate ATP-dependent hydrogen ion Transport. The soy isoflavone genistein and the benzoquinonoid antibiotic herbimycin inhibited hydrochloric Acid Transport with 50% inhibition at 10 and 2 μmol/L, respectively: effects appeared in 20 μmol/L. We conclude that tyrosine kinase inhibition directly inhibits osteoclast membrane hydrochloric Acid Transport: differences among inhibitors may reflect chemical reactivity and permeability.

  • Tyrosine kinase inhibitor effects on avian osteoclastic Acid Transport.
    The American journal of clinical nutrition, 1998
    Co-Authors: J P Williams, S E Jordan, S Barnes, H C Blair
    Abstract:

    We found that tyrosine kinase pp60(c-src) coisolates with Acid-Transporting osteoclast membranes and hypothesized that this kinase regulates hydrochloric Acid Transport. We assayed the membrane Acid Transport and bone degradation effects of tyrosine kinase inhibitors in avian osteoclasts. Isoflavone, tyrphostin, and benzoquinonoid inhibitors were compared with inactive analogues to determine nonspecific effects. Acid-secreting membranes, isolated by nitrogen cavitation, were assayed as reconstituted vesicles by using acridine orange to indicate ATP-dependent hydrogen ion Transport. The soy isoflavone genistein and the benzoquinonoid antibiotic herbimycin inhibited hydrochloric Acid Transport with 50% inhibition at approximately 10 and approximately 2 micromol/L, respectively; effects appeared in 20 micromol/L. We conclude that tyrosine kinase inhibition directly inhibits osteoclast membrane hydrochloric Acid Transport; differences among inhibitors may reflect chemical reactivity and permeability.

Richard H. Moseley - One of the best experts on this subject based on the ideXlab platform.

  • Effect of thiazolidinediones on bile Acid Transport in rat liver.
    Life sciences, 2006
    Co-Authors: Kris L. Snow, Richard H. Moseley
    Abstract:

    Abstract The thiazolidinedione derivatives, troglitazone, rosiglitazone, and pioglitazone, are novel insulin-sensitizing drugs that are useful in the treatment of type 2 diabetes. However, hepatotoxicity associated with troglitazone led to its withdrawal from the market in March 2000. In view of case reports of hepatotoxicity from rosiglitazone and pioglitazone, it is unclear whether thiazolidinediones as a class are associated with hepatotoxicity. Although the mechanism of troglitazone-associated hepatotoxicity has not been elucidated, troglitazone and its major metabolite, troglitazone sulfate, competitively inhibit adenosine triphosphate (ATP)-dependent taurocholate Transport in isolated rat canalicular liver plasma membrane vesicles mediated by the canalicular bile salt export pump (Bsep). These results suggest that cholestasis may be a factor in troglitazone-associated hepatotoxicity. To determine whether this effect is 1) limited to canalicular bile Acid Transport and 2) is specific to troglitazone, the effect of troglitazone, rosiglitazone, and ciglitazone on bile Acid Transport was examined in rat basolateral (blLPM) and canalicular (cLPM) liver plasma membrane vesicles. In cLPM vesicles, troglitazone, rosiglitazone, and ciglitazone (100 μM) all significantly inhibited ATP-dependent taurocholate Transport. In blLPM vesicles, these three thiazolidinediones also significantly inhibited Na + -dependent taurocholate Transport. Inhibition of bile Acid Transport was concentration dependent and competitive in both cLPM and blLPM vesicles. In conclusion, these findings are consistent with a class effect by thiazolidinediones on hepatic bile Acid Transport. If hepatotoxicity is associated with this effect, then hepatotoxicity is not limited to troglitazone. Alternatively, if hepatotoxicity is limited to troglitazone, other mechanisms are responsible for its reported hepatotoxicity.

  • Hepatic amino Acid Transport.
    Seminars in liver disease, 1996
    Co-Authors: Richard H. Moseley
    Abstract:

    Significant progress has been made in the molecular characterization of the hepatic amino Acid Transport systems, processes that play a key role in hepatocellular functions such as gluconeogenesis and glycogen formation, and the response of the hepatocyte to injury. Several amino Acid Transporters have been cloned, and regulation of hepatic amino Acid Transport under normal and pathophysiologic conditions can now be examined in greater detail. Recent work on the hepatic amino Acid Transport systems is reviewed, and the clinical implications of these findings, if known, are discussed.